Vascular endothelial cell growth factor receptor 3-mediated activation of lymphatic endothelium is crucial for tumor cell entry and spread via lymphatic vessels
Lymphangiogenic growth factors vascular endothelial growth factor (VEGF)-C and VEGF-D have been shown to promote lymphatic metastasis by inducing tumor-associated lymphangiogenesis. In this study, we have investigated how tumor cells gain access into lymphatic vessels and at what stage tumor cells initiate metastasis. We show that VEGF-C produced by tumor cells induced extensive lymphatic sprouting towards the tumor cells as well as dilation of the draining lymphatic vessels, suggesting an active role of lymphatic endothelial cells in lymphatic metastasis. A significant increase in lymphatic vessel growth occurred between 2 and 3 weeks after tumor xenotransplantation, and lymph node metastasis occurred at the same stage. These processes were blocked dose-dependently by inhibition of VEGF receptor 3 (VEGFR-3) signaling by systemic delivery of a soluble VEGFR-3-immunoglobulin (Ig) fusion protein via adenoviral or adeno-associated viral vectors. However, VEGFR-3-Ig did not suppress lymph
%0 Journal Article
%1 He.2005
%A He, Y.
%A Rajantie, I.
%A Pajusola, K.
%A Jeltsch, M.
%A Holopainen, T.
%A Yla-Herttuala, S.
%A Harding, T.
%A Jooss, K.
%A Takahashi, T.
%A Alitalo, K.
%D 2005
%J Cancer Res.
%K & Adenoviridae Animals Antitumor Assays Cell Cells Endothelial Endothelium Factor Fusion Genetic Growth Humans Immunoglobulins Laboratories Line Lung Lymph Lymphangiogenesis Lymphatic Metastasis Mice Model Neoplasm Neoplasms Neovascularization Nodes Pathologic Proteins Receptor-3 Recombinant Research Scid Signal Staging Transduction Tumor Vascular Vectors Vessels Xenograft administration antagonists cells control dosage genetics inhibitors pathology physiology prevention protein therapy
%N 11
%P 4739-4746
%T Vascular endothelial cell growth factor receptor 3-mediated activation of lymphatic endothelium is crucial for tumor cell entry and spread via lymphatic vessels
%U PM:15930292
%V 65
%X Lymphangiogenic growth factors vascular endothelial growth factor (VEGF)-C and VEGF-D have been shown to promote lymphatic metastasis by inducing tumor-associated lymphangiogenesis. In this study, we have investigated how tumor cells gain access into lymphatic vessels and at what stage tumor cells initiate metastasis. We show that VEGF-C produced by tumor cells induced extensive lymphatic sprouting towards the tumor cells as well as dilation of the draining lymphatic vessels, suggesting an active role of lymphatic endothelial cells in lymphatic metastasis. A significant increase in lymphatic vessel growth occurred between 2 and 3 weeks after tumor xenotransplantation, and lymph node metastasis occurred at the same stage. These processes were blocked dose-dependently by inhibition of VEGF receptor 3 (VEGFR-3) signaling by systemic delivery of a soluble VEGFR-3-immunoglobulin (Ig) fusion protein via adenoviral or adeno-associated viral vectors. However, VEGFR-3-Ig did not suppress lymph
@article{He.2005,
abstract = {Lymphangiogenic growth factors vascular endothelial growth factor (VEGF)-C and VEGF-D have been shown to promote lymphatic metastasis by inducing tumor-associated lymphangiogenesis. In this study, we have investigated how tumor cells gain access into lymphatic vessels and at what stage tumor cells initiate metastasis. We show that VEGF-C produced by tumor cells induced extensive lymphatic sprouting towards the tumor cells as well as dilation of the draining lymphatic vessels, suggesting an active role of lymphatic endothelial cells in lymphatic metastasis. A significant increase in lymphatic vessel growth occurred between 2 and 3 weeks after tumor xenotransplantation, and lymph node metastasis occurred at the same stage. These processes were blocked dose-dependently by inhibition of VEGF receptor 3 (VEGFR-3) signaling by systemic delivery of a soluble VEGFR-3-immunoglobulin (Ig) fusion protein via adenoviral or adeno-associated viral vectors. However, VEGFR-3-Ig did not suppress lymph },
added-at = {2010-02-05T11:28:39.000+0100},
author = {He, Y. and Rajantie, I. and Pajusola, K. and Jeltsch, M. and Holopainen, T. and Yla-Herttuala, S. and Harding, T. and Jooss, K. and Takahashi, T. and Alitalo, K.},
biburl = {https://www.bibsonomy.org/bibtex/21e6f63e4e13c562e65844b4fd1b765ea/kanefendt},
interhash = {26afe0445ba4a9fdfbe79d1bcc4545f7},
intrahash = {1e6f63e4e13c562e65844b4fd1b765ea},
journal = {Cancer Res.},
keywords = {& Adenoviridae Animals Antitumor Assays Cell Cells Endothelial Endothelium Factor Fusion Genetic Growth Humans Immunoglobulins Laboratories Line Lung Lymph Lymphangiogenesis Lymphatic Metastasis Mice Model Neoplasm Neoplasms Neovascularization Nodes Pathologic Proteins Receptor-3 Recombinant Research Scid Signal Staging Transduction Tumor Vascular Vectors Vessels Xenograft administration antagonists cells control dosage genetics inhibitors pathology physiology prevention protein therapy},
number = 11,
pages = {4739-4746},
timestamp = {2010-02-05T11:28:41.000+0100},
title = {Vascular endothelial cell growth factor receptor 3-mediated activation of lymphatic endothelium is crucial for tumor cell entry and spread via lymphatic vessels},
url = {PM:15930292},
volume = 65,
year = 2005
}